Paramecia show chemokinesis, that is, they accumulate in or disperse away from chemicals. The cells perform this behavior by changing their ciliary motion, which changes the frequency of random turns and the speed of swimming. The described project approaches Paramecium chemokinesis as a chemosensory transduction pathway in which external chemical cues are detected by the cells, the cells alter their swimming in response, and these alterations cause populations of cells to accumulate or disperse. Mutants are presently being used by the Principal Investigator to study the effects of blocks in this chemosensory pathway from the receptor end (possibly the cell membrane) to the effector end (the cilia). The proposed research includes the isolation of more mutants with general or specific defects in chemokinesis behavior and their use in examining: 1) ciliary beating and the motile mechanisms that lead to accumulation or dispersal of populations; 2) the membrane electrical correlates of chemokinesis; 3) the organization of genes that control a behavior; 4) and the association of an attractant with the cell membrane, the putative receptor end of the pathway. Electrophysiological study is included in this genetic dissection because the movement of cilia, and hence swimming behavior, is under membrane electrical control. Cells defective in membrane electrogenesis have been used in this study and more are expected among the new chemokinesis defective mutants. An hypothesis of membrane potential control of chemokinesis has been developed by the Principal Investigator and will be tested in the proposed project. Other methods include videotape analysis of swimming behavior, genetic crosses, and isotope incorporation assays.